Using grease-gap recording from rat neocortical slices, the γ-aminobutyric acid B (GABA B ) receptor agonists baclofen (3–100 μM) and SKF 97541 (3-aminopropyl-methylphosphinic acid) (1–30 μM) elicited reversible and concentration-dependent hyperpolarizing responses, with EC 50 values of 10 and 3 μM, respectively. The hyperpolarizations were antagonised by the GABA B receptor antagonist Sch 50911 ((+)-( S )-5,5-dimethylmorpholinyl-2-acetic acid) (1, 5 and 10 μM). Fendiline ( N -(3,3-diphenylpropyl)-α-methylbenzylamine) (5–50 μM) and its congeners, prenylamine ( N -(3,3-diphenylpropyl)-α-methylphenylethylamine) (10–100 μM) and F551 ( N -(3,3-diphenylpropyl)-α-methyl-3-methoxybenzylamine) (1–30 μM) reversibly enhanced hyperpolarizing responses to the agonists; such effects were reduced by Sch 50911. These arylalkylamines produced leftward shifts of the concentration–response curves, with a marked increase in the maximal hyperpolarization obtained, compared with the agonists alone, F551 being the most potent. These findings suggest that these arylalkylamines represent a new class of positive modulators of GABA B receptor-mediated function.
European Journal of Pharmacology – Elsevier
Published: Sep 6, 2002
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